دورية أكاديمية
أعرض في EDS

Autophagy Protects against Eosinophil Cytolysis and Release of DNA.

التفاصيل البيبلوغرافية
العنوان: Autophagy Protects against Eosinophil Cytolysis and Release of DNA.
المؤلفون: Esnault S; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Fichtinger PS; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Barretto KT; Department of Biomolecular Chemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Fogerty FJ; Department of Biomolecular Chemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Bernau K; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Mosher DF; Department of Biomolecular Chemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA.; Division of Hematology and Oncology, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Mathur SK; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Sandbo N; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA., Jarjour NN; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI 53726, USA.
المصدر: Cells [Cells] 2022 Jun 02; Vol. 11 (11). Date of Electronic Publication: 2022 Jun 02.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: Eosinophils* , Interleukin-5*, Autophagy ; DNA ; Immunoglobulin G
مستخلص: The presence of eosinophils in the airway is associated with asthma severity and risk of exacerbations. Eosinophils deposit their damaging products in airway tissue, likely by degranulation and cytolysis. We previously showed that priming blood eosinophils with IL3 strongly increased their cytolysis on aggregated IgG. Conversely, IL5 priming did not result in significant eosinophil cytolysis in the same condition. Therefore, to identify critical events protecting eosinophils from cell cytolysis, we examined the differential intracellular events between IL5- and IL3-primed eosinophils interacting with IgG. We showed that both IL3 and IL5 priming increased the eosinophil adhesion to IgG, phosphorylation of p38, and production of reactive oxygen species (ROS), and decreased the phosphorylation of cofilin. However, autophagic flux as measured by the quantification of SQSTM1-p62 and lipidated-MAP1L3CB over time on IgG, with or without bafilomycin-A1, was higher in IL5-primed compared to IL3-primed eosinophils. In addition, treatment with bafilomycin-A1, an inhibitor of granule acidification and autophagolysosome formation, enhanced eosinophil cytolysis and DNA trap formation in IL5-primed eosinophils. Therefore, this study suggests that increased autophagy in eosinophils protects from cytolysis and the release of DNA, and thus limits the discharge of damaging intracellular eosinophilic contents.
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معلومات مُعتمدة: R01 HL146402 United States HL NHLBI NIH HHS; UL1 TR002373 United States TR NCATS NIH HHS; P01 HL088594 United States HL NHLBI NIH HHS; UL1 RR025011 United States RR NCRR NIH HHS
فهرسة مساهمة: Keywords: DNA traps; IL3; IL5; IgG; MAP1LC3B; SQSTM1; autophagy; cytolysis; eosinophils
المشرفين على المادة: 0 (Immunoglobulin G)
0 (Interleukin-5)
9007-49-2 (DNA)
تواريخ الأحداث: Date Created: 20220610 Date Completed: 20220613 Latest Revision: 20230207
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9180302
DOI: 10.3390/cells11111821
PMID: 35681515
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells11111821